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http://dx.doi.org/10.3345/kjp.2010.53.4.525

Apoptosis and upregulation of TNF-${\alpha}$ and TRAIL receptor 1 (DR4) in the pathogenesis of food protein-induced enterocolitis syndrome  

Hwang, Jin-Bok (Department of Pediatrics, Keimyung University School of Medicine)
Kim, Sang-Pyo (Department of Pathology, Keimyung University School of Medicine)
Kang, Yu-Na (Department of Pathology, Keimyung University School of Medicine)
Lee, Seong-Ryong (Department of Institute for Medical Science, Keimyung University School of Medicine)
Suh, Seong-Il (Department of Institute for Medical Science, Keimyung University School of Medicine)
Kwon, Taeg-Kyu (Department of Institute for Medical Science, Keimyung University School of Medicine)
Publication Information
Clinical and Experimental Pediatrics / v.53, no.4, 2010 , pp. 525-531 More about this Journal
Abstract
Purpose : Expression levels of tumor necrosis factor (TNF)-${\alpha}$ expression on the mucosa of the small intestine is increased in patients with villous atrophy in food protein-induced enterocolitis syndrome (FPIES). TNF-${\alpha}$ has been reported to induce apoptotic cell death in the epithelial cells. We studied the TNF family and TNF-receptor family apoptosis on the duodenal mucosa to investigate their roles in the pathogenesis of FPIES. Methods : Fifteen infants diagnosed as having FPIES using standard oral challenge test and 5 controls were included. Terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining was performed to identify the apoptotic cell death bodies. Immunohistochemical staining of TNF-${\alpha}$, Fas ligand (FasL) for TNF family and TNF-related apoptosis-including ligand (TRAIL) receptor 1 (DR4), TRAIL receptor 2 (DR5), and Fas for TNF-receptor family were performed to determine the apoptotic mechanisms. Results : $TUNEL^+$ was significantly more highly expressed in the duodenal mucosa of FPIES patients than in controls ($P$-0.043). TNF-${\alpha}$ ($P$=0.0001) and DR4 ($P$=0.003) were significantly more highly expressed in FPIES patients than in controls. Expression levels of FasL, Fas, and DR5 were low in both groups and were not significantly different between the 2 groups. Conclusion : These results suggest that FPIES pathogenesis is induced by apoptosis, and that TNF-${\alpha}$ expression and DR4 pathway may have an important role in apoptosis.
Keywords
Food protein-induced enterocolitis syndrome; Etiology; Apoptosis; Tumor necrosis factor-alpha; TNF-related apoptosis-including ligand receptor 1;
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